RESPONSE TO LINDBERG ET AL.’S AND WARD’S COMMENTARIES

We thank Lindberg et al. and Ward for their comments on our paper “Spasticity or reversible hypertonia”. In response to Lindberg et al’s remarks, we wish to reiterate that the validity of Lance’s definition (1) and the neural origin of spasticity are not disputed by us, nor does our proposed definition exclude the co-existence of spasticity with the other factors that contribute to the clinically demonstrable hypertonia. The fundamental point in our discourse is that “pure” spasticity, as defined by Lance, i.e. hyperexcitability of the spinal alpha motor neurones in the absence of changes in the viscoelastic properties and structure of muscle, is a transient phenomenon, at least in most patients with an upper motor neurone lesion. Furthermore, as Lindberg et al. have conceded, the frequency of occurrence, the trajectory of evolution and the relevance of the H-reflex changes over time do not follow a consistent pattern. Therefore, given the transient nature of spasticity and its doubtful contribution to the long-term motor disability in these patients, we would argue that the use of the term hypertonia is a more appropriate and pragmatic description of the clinical situation, as it includes all the factors that are known to cause the resistance to muscle stretch. The addition of “reversible” in our proposed definition is meant to indicate that the hypertonia is amenable to conservative medical interventions. In other words, it means that a significant fixed shortening of the muscle-tendon unit (that requires surgery) has not set in. The use of “reversible” in this context is not intended to suggest that the changes in the H-reflex reduce over time, as implied in Lindberg et al.’s commentary.

Lindberg et al. rightly state that the term spasticity is “used clinically as an umbrella term to describe all these [dystonia, co-contraction, etc.] forms of muscle overactivity.” We also agree with them that “unclear terminology can cause confusion between clinicians and make it difficult to interpret scientific results”. However, we believe their proposal that the term “spasticity” should be used routinely in clinical practice contradicts the latter statement. They also suggest that Lance’s definition (1) should be used for spasticity, and that “the mechanical resistance in muscle” is defined separately. As the increased excitability of the spinal alpha motor neurones and the structural muscle changes exist simultaneously it is difficult to understand how the two separate definitions for the same medical impairment enable a coherent approach to diagnosis and treatment.

The purpose of our proposed definition is to emphasise the component of muscle hypertonia, that is likely to respond to conservative medical “antispasticity” treatment. We believe that the main value of this definition is that it does not capture all presentations of the upper motor neurone syndrome. Indeed, as Ward stated it is not desirable to use terminology that describes all manifestations of an upper motor neurone lesion because the disability resulting from it can be due to poor motor control rather than spasticity. The term “spasticity” does not allow clinicians to make this distinction.

Reference

Abdel Magid O. Bakheit, MD, PhD1, Klemens Fheodoroff, MD2 and Franco Molteni, MD3

From the 1Moseley Hall Hospital, Birmingham, UK,
2Gailtal Klinik, Hermagor, Austria and 3Villa Beretta,
Costamasnaga, Italy